PREDISPOSING FACTORS TRANSIENT ISCHEMIC ATTACK PRECIPITATING FACTORS
PATHOPHYSIOLOGY Hypertension
Age
Heredity Diabetes mellitus
Sex Undesirable levels of
cholesterol
Poor diet
Physical inactivity
LEGEND
Disease process
Signs and symptoms
Nursing Dx
Nursing Management
Toxic irritants from tobacco damages the
Medical Management
endothelium
Surgical Management
Not Treated
Treated
Damage becomes site for atherosclerosis
Diagnostic tests
Lab results
Formation of plaque deposit, a buildup of fats, Platelets adhere to the
May lead to embolism cholesterol, proteins, calcium and immune cells thrombogenic plaque causing
obstructs arterial blood flow complete blockage of the artery.
GLUCOSE – 121.3 mg/Dl
Obstruction of blood flow Narrowing of blood vessels Cholesterol – 221.6 atorvastatin
mg/dL
Deficient knowledge Hypertension Increase pressure in the blood vessels
Problem-solve with the patient to Death of some neurons in the ischemic
identify ways appropriate lifestyle core while some can still be restored in
changes can reduce modifiable risk the ischemic penumbra
factors.
Losartan
CVD (Stroke) MRI, CT SCAN
Clonidine
Amlodipine
If NOT treated If treated
Carotid endarterectomy
Cerebral ischemia Weakness in one arm or leg Craniectomy and hemispheric
dizziness decompression
Slurred speech
Initiation of ischemic cascade
Anti-platelet drugs
anticoagulants
Ineffective Cerebral Tissue
High buildup of sodium and Perfusion
calcium in the cell.
• Check rapid changes or
High sodium level draws water into continued shifts in mental Good cerebral perfusion
the cell called cytotoxic edema status.
• Initiation of FAST
Pallative care
High calcium leads up to build up Na -143.9 mmol/L
Frequent vital sign and
of reactive oxygen radicals K – 3.12 mmol/L neuro vital sign
Damage lipids in the mitochondria Good improvement
and lysosomes
Release of apoptosis inducing GOOD PROGNOSIS
factors and degradative enzymes
• Lymphocytes 41.3
• Eosinophils 12.g
Inflammation damages blood brain barrier
\ allowing fluids and proteins into the cell causing
vasogenic edema.
Blood tests
Altered cerebral metabolism and decrease cerebral perfusion
Damage of the hemisphere of the brain Increase Intracranial Pressure
Impaired perfusion and function
Numbness on the feet left side of the brain, trouble speaking, difficulty of walking, dizziness and
sudden severe headache
Impaired Verbal Space occupying blood clot put more pressure
Communication on the brain
• Ask the patient to follow simple Excessive anoxic brain damage
commands (“Close and open your
eyes,” “Raise your hand”); repeat
simple words or sentences.
Cardiac arrest
• Ask the patient to write their name
and a short sentence. If unable to
write, have the patient read a short
sentence. Multiple organ dysfunction
• Provide alternative methods of
communication.
DEATH
Using Tenecteplase for Acute Ischemic Stroke: What Is the Hold Up?
Tony Zitek, MD, Ramsey Ataya, MD, and Isabel Brea, MD
Abstract
Alteplase is the only Food and Drug Administration-approved intravenous (IV) thrombolytic medication for acute ischemic stroke. However, multiple
recent studies comparing tenecteplase and alteplase suggest that tenecteplase is at least as efficacious as alteplase with regards to neurologic
improvement. When given at 0.25 milligrams per kilogram (mg/kg), tenecteplase may have less bleeding complications than alteplase as well. This
narrative review evaluates the literature and addresses the practical issues with regards to the use of tenecteplase versus alteplase for acute
ischemic stroke, and it recommends that physicians consider tenecteplase rather than alteplase for thrombolysis of acute ischemic stroke.
Neurologic improvement after stroke
The results of five randomized controlled trials have been published that compare alteplase and tenecteplase for acute ischemic stroke.7–11 The first
was by Haley et al, published in 2010,7 and it randomized patients with suspected acute ischemic stroke within 3 hours to tenecteplase 0.1
milligrams per kilogram (mg/kg), tenecteplase 0.25 mg/kg, tenecteplase 0.4 mg/kg, or standard dose alteplase (0.9 mg/kg). Patients in the
tenecteplase 0.4 mg/kg group had the lowest rate of good neurologic outcomes at three months (defined as modified Rankin scale score of 0 or 1).
There were no statistically significant differences among the other groups, but there was a trend towards higher percentages of patients having good
neurologic outcomes in the tenecteplase 0.1 mg/kg and 0.25 mg/kg groups as compared to the alteplase group: tenecteplase 0.1 mg/kg 45.2%,
tenecteplase 0.25 mg/kg 48.4%, and alteplase 41.9%
Conclusion
Tenecteplase is at least as effective as alteplase with regards to neurologic improvement after treatment of acute ischemic stroke. Additionally,
tenecteplase is less expensive, easier to administer, and may have less bleeding complications than alteplase. Thus, physicians should consider
using tenecteplase rather than alteplase for thrombolysis of acute ischemic stroke. If used, the preferred dose of tenecteplase is 0.25 mg/kg
(maximum 25 mg).